Impact of RNA Virus Evolution on Quasispecies Formation and Virulence

Abstract

RNA viruses are known to replicate by low fidelity polymerases and have high mutation rates whereby the resulting virus population tends to exist as a distribution of mutants. In this review, we aim to explore how genetic events such as spontaneous mutations could alter the genomic organization of RNA viruses in such a way that they impact virus replications and plaque morphology. The phenomenon of quasispecies within a viral population is also discussed to reflect virulence and its implications for RNA viruses. An understanding of how such events occur will provide further evidence about whether there are molecular determinants for plaque morphology of RNA viruses or whether different plaque phenotypes arise due to the presence of quasispecies within a population. Ultimately this review gives an insight into whether the intrinsically high error rates due to the low fidelity of RNA polymerases is responsible for the variation in plaque morphology and diversity in virulence. This can be a useful tool in characterizing mechanisms that facilitate virus adaptation and evolution.

Animal and human RNA viruses: genetic variability and ability to overcome vaccines

“…In general, the fact that RNA viruses display greater substitution rates than their DNA counterparts is mainly due the low fidelity of the RNA polymerases, which usually lack a proofreading mechanism and have high mutation rates. This lack of replication fidelity, together with the fact that RNA viruses can undergo spontaneous mutations, results in genetic variants displaying different viral morphogenesis and variation on their surface glycoproteins, that affect the viral antigenicity and can result in the production of viral quasispecies (Mandary et al 2019 ).…”

“…The quasispecies phenomenon could also be responsible for the differences in virulence, as well as plaque size and morphology, found in RNA viruses, and these studies are important to determine if severe infections are caused by a single strain or are the result of the cooperative effect of viral quasispecies, displaying different mutations. This information would give an important insight into virus evolution and adaptation, as well as positively contributing to the design of more effective, and longer-lasting, vaccines against RNA viruses (Mandary et al 2019 ).…”

“…1 Graphic representation of the 10 human viruses described in the text (creative common licence figures from VIPERdb https ://viper db.scrip ps.edu (Carrillo-Tripp et al 2009) and Reddy et al 2015). The virus families included here are: a Picornaviridae, b Coronaviridae, c Caliciviridae, d Astroviridae, e Togaviridae, f Bunyaviridae, g Rhadoviridae, h Filoviridae, i Orthomyxoviridae, and j Paramyxoviridae Table 1 Characteristics of the main ssRNA human virus families (Dietzgen et al 2017;Kuhn et al 2019;Rima et al 2019;Chen et al 2018;Vinjé et al 2019;Zell et al 2017;Mandary et al…”

Structures and Functions of Viral 5′ Non-Coding Genomic RNA Domain-I in Group-B Enterovirus Infections

“…EV-B are well known for their high genomic plasticity mainly related to the lack of proofreading activity of the 3D pol resulting in approximately one mutation per 10 3 -10 5 copied nt [109] in every new genome generated during replication phase [110]. The acquisition of mutations (insertions, substitutions, or deletions) allows the generation of a set of viral sub-populations characterized in quasi-species [111,112]. Among these quasi-species, major EV-B populations were shown to contain 5 terminal deletions ranging up to 49 nt, increasing in deletion size inside RNA domain-I over viral culture passage or time post-infection in experimental models [113].…”

Structures and Functions of Viral 5’ Non-Coding Genomic RNA Domain-I in Enterovirus-B Infections

“…copied nt [109] in every new genome generated during replication phase [110]. The acquisition of mutations (insertions, substitutions or deletions) allows the generation of a set of viral sub-populations characterized in quasi-species [111,112]. Among these quasi-species, major EV-B populations were shown to contain 5'terminal deletions ranging up to 49 nt , increasing in deletion size inside RNA domain-I over viral culture passage or time post-infection in experimental models [113].…”